The electrophysiological effects of capsaicin in rat atrial myocytes were examined. Measurement of contractile force was done in rat left atria. Whole-cell patch-clamp technique was primarily used to study the change in membrane potential and ionic currents. Capsaicin produced an initial rise and a sustained increase in contractile force in rat left atria. Capsaicin (10 μM) caused a significant prolongation of atrial action potential. In voltage-clamp experiments, capsaicin (1-100 μM) caused the reversible reduction in the amplitude of transient outward (I(TO)) and late outward (I(L)) K(+) currents in concentration- and voltage-dependent manners. The time course for inactivation of I(TO) was changed to the biexponential process after the application of capsaicin. Capsaicin failed to cause any significant shift in quasi-steady-state inactivation curve of I(TO). The EC(50) values for the inhibitory effects of capsaicin on I(TO) and I(L) were 5 and 20 μM, respectively. Capsaicin also suppressed the amplitude of acetylcholine- or adenosine-induced K(+) current, i.e., I(K(ACh,Ado)). The EC(50) value for capsaicin-mediated inhibition of I(K(ACh,Ado)) is 50 μM. The present findings suggest that in isolated rat atria, during capsaicin exposure, the capsaicin-mediated inhibition of these K(+) channels is one of the ionic mechanisms underlying the positive inotropic and chronotropic actions.